2. âNo head injury is so serious that it should be despaired of nor
so trivial that it can be ignoredâ
- âThe aphorisms of Hippocratesâ(1817)
3. Overview
⢠The problem statement
⢠Pathophysiology
⢠Pre-hospital management
⢠Monitoring in TBI
⢠Critical care management
⢠Guidelines for TBI
⢠Current evidence in TBI
⢠Prognostication
⢠Summary
4. The problem statement
⢠TBI leading cause of death and disability in the age group of 1-
44 in the USA
⢠Estimated 1.5million head injuries in the US annually
⢠Estimated 50000 deaths every year in the US
⢠Male: Female: 1.5-2:1
⢠Increased risk of persistent neurological deficits and severe
disability
⢠50% due to RTAs; 33% due to falls and 10% due to
recreational activities
Data from the Brain Trauma Foundation
5. The Indian Picture
⢠1million injured annually
⢠200000 deaths a year
⢠Bangalore: 10000 injuries/year
⢠1000 deaths annually
⢠RTAs major cause; 25% falls and 10% violence related
⢠Most common age group: 15-40, the productive workforce
⢠71% mild; 15% moderate and 13% severe TBI
Data from NIMHANS(www.nimhans.kar.nic.in/epidemiology/doc/ep_ft25.pdf)
9. Pathophysiology
⢠Primary injury- physical damage occurring to parenchyma(tissue or
vessels)
- shear and compression of surrounding brain tissue
⢠Secondary injury (causes are intuitive)
-Hypoxemia, hypo/hypercapnia
-Hypotension/hypertension
-Seizures/Infection
-increases in ICP
-hypo/hyperglycemia
-anemia
⢠Disruption in autoregulation
⢠Polytrauma and other organ damage/dysfunction
10. Secondary Injury
⢠Most common cause is âICP
⢠Vasogenic edema
⢠CPP: MAP-ICP
⢠Concomitant decreases in MAP-further ischemia
⢠Herniation and mortality
11. Secondary Injury
⢠Hypoxemia and hypotension
⢠Common prior to arrival of the patient to the hospital
⢠27-55% of patients hypoxemic at the scene, in the ambulance
or on arrival to ER
⢠Early intubation when indicated
⢠Monitoring Sats and BP
⢠Early goal directed therapy
⢠Efficient and trained paramedical services
⢠One episode of hypotension can almost double the mortality
12. Management
⢠Pre-hospital
- requires trained paramedical and ER personnel
- requires organizational support(trauma centers/ER)
⢠Hospital management and guidelines
- ICU management of TBI
15. Organizational Structure
⢠Emergency Room and ICU in a tertiary care hospital
⢠Trauma Centers
- Level1
- Level 2
- Level 3
- Level 4
- Level 5
⢠India: National Level-AIIMS and PGI
⢠Karnataka: Sanjay Gandhi Trauma Center
16. Pre-hospital care-Guideline Based
⢠50% of deaths within 2hrs
⢠Improved pre-hospital and ER care-better outcomes
⢠Oxygenation and Blood Pressure:
- Level of evidence: weak
- monitoring for Sats and BP
- continual monitoring
- maintaining satsâş90% and SBPâş90mm
⢠Traumatic Coma Data Bank: 717 patients- hypoxemia and
hypotension among the 5most powerful predictors of
outcome
Source: Brain Trauma Foundation
17. ⢠Assessment: Level of evidence-weak
- Measuring GCS is a reliable indicator of TBI
- Repeat measurements of GCS
- GCS to be measured after A, B and C
- prior to administering sedatives/paralytics or after washout
- fair correlation with mortality when taken in context
- Assessment of pupils: level of evidence weak
- to be done after resuscitation and stabilization
- asymmetry: more than 1mm difference between pupils
- fixed: less than 1mm response to bright light
18. ⢠Treatment
⢠Ventilation and oxygenation: Level of evidence-weak
- Preventing hypoxemia
- early securement of airway in severe TBI
- RSI
- Confirmation of ET including EtCO2
- Normal ventilation(PaCO2:35-45)
- Avoid hyperventilation unless imminent cerebral herniation
19. ⢠Fluid resuscitation: Level of evidence-weak
- Hypotensive patients to be resuscitated with isotonic fluids
- Consider hypertonic fluids in the setting of severe TBI
⢠Imminent herniation: Level-weak
- Mild or prophylactic hyperventilation to be avoided
- only if there are imminent signs
- asymmetric pupils, dilated and unreactive pupils, motor
extensor posturing and worsening GCS
- hyperventilation as a temporizing measure
20. Critical care management
⢠Stabilization of patient, if still unstable
⢠Prevention of any increases in ICP
⢠Maintaining an adequate and stable CPP
⢠Avoidance of secondary insults
⢠Optimization of cerebral hemodynamics and oxygenation
⢠Operative strategies when required
22. Monitoring
⢠General monitoring
-ECG
-Pulse oximetry
-Capnography
-Arterial pressure monitoring
-CVP
-Urine output
-Serum electrolytes and osmolality
-ABGs
23. Neuromonitoring
⢠ICP monitoring: No level 1 evidence to support routine use
- However level 2 evidence present
- In all salvageable patients with GCS between 3-8 with
abnormal CT
- In the presence of a normal CT if:
1. ageâş40years
2. unilateral/bilateral motor posturing
3. SBPâš90mm
⢠Independent predictor of mortality
Source: BTF guidelines 3rd Ed.
24.
25. ⢠Different methods- subdural, subarachnoid, epidural,
intraventricular, parenchymal
⢠Intraventricular most accurate, low cost and reliable
⢠Also can drain the CSF in the event of very high pressure
⢠Usually placed on the right side; may also be placed on the
side with maximum pathological features
⢠Incidence of infection-11%
⢠Routine change of catheter not recommended
⢠Antibiotic prophylaxis not recommended
⢠Usually for less than a week
26.
27. ICP waveforms
⢠Lundberg and colleagues in 1965
⢠Three primary wave forms
⢠A waves: steep increases from baseline to 50-80mm
- always pathologic
- associated with early signs of herniation
- represents phasic vasodilatation in response to decreased
CPP
⢠B waves: rhythmic oscillations occurring at 0.5-2waves/min
- peak ICP of 20-30mm
- Due to changes in vasomotor tone
⢠C waves: Max ICP upto 20mm; not clinically relevant
28.
29.
30. Neuromonitoring
⢠Jugular venous bulb oxygen saturation
-indicator of cerebral metabolism and oxygenation
-by retrograde catheterization of IJV
-usually rt.IJV
-continuous using fibreoptic technique/intermittent
-evidence is conflicting
-normal range 55-70%
-less than 50% is the threshold
-d/t hypotension, vasospasm or hypocapnia
-evidence is level 3
31. Neuromonitoring
⢠Brain tissue oxygen tension
-level: level 3 evidence
-âš15mm is threshold for treatment
-monitors focal oxygenation
-invasive probe
-most reliable for monitoring critically perfused tissue
-normal range 35-50mmHg
-several studies have shown improved outcome
-not widely available
32. ⢠Cerebral microdialysis
-recently developed
-invasive
-usually a MD catheter placed into most vulnerable area
-measures biochemical changes in these areas
-measures glucose, lactate, pyruvate, glycerol, glutamate
-âlactate/pyruvate ratio
-value more than 20-25 is threshold
-limited use
33. ⢠Transcranial Doppler
-non invasive method
-useful to detect vasospasm, critical elevations in ICP
-to detect decreases in CPP, brain death
-sensitivity for brain death is 75-88%
-specificity is 98%
-no established role in regular TBI care
⢠Other monitors: EEG, NIRS, Brain temperature monitoring
34. Critical Care Management
⢠Analgesia, sedation and paralysis
⢠Required for intubation, mechanical ventilation, surgical
procedures and ICU procedures
⢠Keeps patient pain free and comfortable
⢠Avoids increases in ICP associated with agitation, cough
⢠Decrease the CMRO2 and oxygen consumption
⢠Ideal agent: short acting, easily titrated to effect
⢠Propofol, benzodiazepines, opioids
35. ⢠Mechanical ventilation
⢠Severe TBI will usually require intubation and ventilation
⢠Avoid hypoxemia(Satsâš90% and PaO2âš60mm)
⢠No role for prophylactic hyperventilation
⢠Target PaCO2:35-45mm
⢠Consider brief periods if acute deterioration
⢠Adequate sedation for intubation/suctioning
⢠Role of PEEP?
⢠ALI/ARDS with TBI-Major challenge
36. ⢠Hemodynamic support
⢠Avoid hypotension
⢠Causes: Polytrauma, spinal injuries, myocardial contusion
⢠Target MAP of 80mm if ICP monitoring is not in place
⢠CPP of 60-70mm
⢠Adequate fluid resuscitation-CVP/PCWP/SPV/PPV guided
⢠Vasopressors as indicated-avoid Dopamine
⢠Correct anemia-transfusion threshold??
⢠Avoid hypertension as it can increase vasogenic edema
37. ⢠Hyperosmolar therapy
⢠Mannitol and Hypertonic saline
⢠Osmotic diuresis with mannitol
⢠Monitor serum osmolarity(target 320)
⢠Adequate fluid resuscitation and euvolemia
⢠Hypertonic saline-safe, effective
⢠Expands intravascular volume, decreases ICP
⢠Generally free of adverse effects such as renal
failure/pulmonary edema
⢠Avoid mannitol in patients with renal failure
38. ⢠Hypothermia
⢠No conclusive evidence to support role of hypothermia
⢠Fever to be aggressively controlled
⢠Antiseizure prophylaxis
⢠Early versus late post traumatic seizures
⢠Prophylactic therapy not recommended for preventing late
⢠For early if there are risk factors
⢠GCSâš10, cortical contusion, depressed skull fracture, SDH,
EDH, penetrating TBI, intracerebral hematoma, seizures
within 24hrs
39. ⢠DVT prophylaxis
⢠High risk group-20% in the absence of prophylaxis
⢠Mechanical measures at the earliest
⢠In the absence of hemorrhage/other contraindications
consider LMWH/UFH as early as after 48-72hrs
⢠Stress ulcer prophylaxis/Nutrition
⢠Early enteral feeding
⢠Proton pump inhibitors
⢠Glycemic control
⢠Hyper/hypo contribute to poor outcome
⢠Optimal Target:150-180mg/dl?
40. ⢠Steroids
⢠NO ROLE
⢠CRASH trial: unequivocally demonstrated higher mortality
⢠Barbiturate Coma
⢠For refractory intracranial HTN
⢠Mechanism: âCBF, CMRO2, ICP
⢠S/E: Hypotension
⢠Prophylactic administration not recommended
⢠Pentobarbital/Thiopentone
CRASH Trial. Lancet. 2005;365(9475):1957-59
41. ⢠Fluid and Electrolyte
⢠Maintain euvolemia
⢠Hypovolemia independent risk factor for poor outcome
⢠Avoid hypotonic fluids
⢠Accept serum Na 150-155
⢠If Naâş160 and correction is required, go gradually
⢠Hypophosphatemia and hypomagnesaemia are common
42. The Lund Concept
⢠Different approach to manage TBI
⢠Based on physiological models
⢠Some studies have shown improved outcome
⢠ICP targeted goal and Perfusion targeted goal
⢠Perfusion targeted: normovolemia, normal hematocrit and
maintain normal blood oxygenation
⢠ICP targeted: to prevent increases and control ICP
-maintain normal plasma colloid pressure
-decrease capillary pressure by reducing systemic BP
-increase tone of pre-capillary resistance vessels
43. General Intensive Care
⢠Raising head end to 30-45degrees
⢠Head and neck in neutral position
⢠Avoid compression on neck veins
⢠Frequent positioning
⢠Eye care, mouth and skin hygiene
⢠Implementing all evidenced based bundles
⢠Physiotherapy
44. Decompressive Craniectomy
⢠Promising approach to severe intractable intracranial HTN
⢠Decompressive craniectomy and hemicraniectomy
⢠As a life saving procedure
⢠Evidence conflicting though physiological basis sound
⢠Decreases ICP and ICU LOS
⢠No difference in outcome at 6months
46. Levels of evidence
⢠Level 1: From good quality RCTs
⢠Level 2
-moderate quality RCT
-good quality cohort
-good quality case control
⢠Level3
-poor quality RCT
-moderate or poor quality cohort
-moderate or poor quality case control
-case series, databases, registries
47. ⢠Blood pressure and oxygenation
-No level 1 recommendation
-Level2: BP must be monitored and avoid SBPâš90
-Level3: Monitor oxygenation; avoid PaO2âš60
⢠Hyperosmolar therapy
-No level 1
-Level2: Mannitol effective in doses 0.25-1g/kg
-Level3: Restrict use of mannitol prior to ICP monitoring to
select patients with signs of transtentorial herniation or
progressive neurological deterioration
- No recommendation for HSS
48. ⢠Prophylactic hypothermia
- No level1 or level 2
- level 3: greater decrease in mortality risk if hypothermia
maintained for 48hrs
- prophylactic hypothermia associated with higher GOS
⢠Infection prophylaxis
- No level1
- Level 2: Periprocedural antibiotics for intubation
- Early tracheostomy to reduce days of ventilation
- Level 3: No routine change of ventricular catheter
- No prophylactic antibiotics for ventricular catheters
49. ⢠DVT prophylaxis
⢠No level 1 or 2
⢠Level 3: Compression stockings or IPD to be used wherever
possible
⢠LMWH to be combined with mechanical methods; higher risk
of expansion of hemorrhage present
⢠Nutrition
⢠No level 1
⢠Level 2: Patients should be fed to attain full calorie
replacement by day 7 post injury
50. ⢠Antiseizure prophylaxis
⢠No level 1
⢠Level 2: prophylactic use of phenytoin not recommended for
preventing late onset seizure
⢠Anticonvulsants are indicated to decrease risk of early post
traumatic seizures(7days)
⢠Early seizures are however not associated with poor
outcomes
⢠Steroids
⢠Level1: Not recommended for improving outcome or âICP
⢠In moderate-severe TBI use is associated withâmortality
51. ⢠Hyperventilation
⢠No level 1
⢠Level 2: prophylactic hyperventilation not
recommended(PaCO2 less than 25)
⢠Recommended as temporizing measure for acute increases in
ICP
⢠Avoid during the first 24hrs when CBF may be critically
reduced
⢠If used, monitor SjvO2 and PbO2
53. ICP monitoring
⢠âA trial of ICP monitoring in TBIâ
⢠NEJM 2012
⢠Multicentre trial for adult TBI
⢠324 patients
⢠Pressure monitoring group or imaging clinical examination
group
⢠Primary outcome a composite of survival time, impaired
consciousness, functional status at 3 and 6 months
⢠Neuropsychological status at 6months
Chestnut et al. N Engl J Med 2012;367:2471-81
54. ⢠No difference in primary outcome
⢠6month mortality in pressure monitoring group 39% versus
imaging clinical examination group 41%(p=0.60)
⢠Median ICU stay was similar(12days in pressure monitoring
versus 9 in imaging)(p=0.25)
⢠Number of days of brain-specific treatments lesser in the
pressure monitoring group
⢠Pressure monitoring based care was not superior to imaging-
clinical exam group
55.
56. Hypothermia
⢠Objective: To estimate the effect of mild hypothermia for TBI
on mortality and long term functional outcomes
⢠RCTs of hypothermia to maximum of 35 degrees
⢠Maintained for at least 12 consecutive hours
⢠Data on death, Glasgow outcome scale and pneumonia
⢠23 trials with 1614 patients
⢠21 trials reported data on deaths
⢠Fewer deaths in patients treated with hypothermia
⢠Only 9 of those had good allocation concealment
⢠In these 9 studies, no difference in mortality seen
57. ⢠21 trials reported data on unfavorable outcomes-death,
severe disability or vegetative state
⢠Again showed better results for hypothermia
⢠In studies with good allocation concealment, less unfavorable
outcomes with hypothermia
⢠However difference was not statistically significant
⢠Hypothermia increased the chances of pneumonia
⢠Only 4 studies with good allocation concealment for
pneumonia
⢠Showed decreased incidence; not statistically significant
58. Hypothermia
⢠âProphylactic hypothermia for TBIâ-a quantitative systematic
review
⢠CJEM 2010
⢠2 groups
⢠Studies with protocol for cooling for predetermined
period(48hrs)
⢠Studies that cooled based on target ICP
⢠No systematic reviews which looked at hypothermia in this
manner
Fox et al. CJEM 2010;12(4):355-64
59. ⢠12 studies with 1327 participants
⢠8 cooled according to long term goal
⢠4 to predetermined end points
⢠In studies with long term ICP targeted cooling, lower mortality
and better neurological outcome
⢠Hypothermia beneficial if started early and if it is directed
towards specific end points
60. Hypothermia
⢠NABIS:H2 Study
⢠To assess if early induction of hypothermia made a difference
⢠Randomized multicentre trial
⢠Non penetrating brain injury enrolled within 2-5hrs
⢠Primary outcome was the Glasgow outcome scale at 6months
⢠Mean time to 35 degrees was 2.6h
⢠To 33 degrees was 4.4h
⢠Outcome was poor in the hypothermia group(RR=1.08)
⢠RR for mortality was 1.30
⢠No utility for hypothermia in severe TBI
Clifton et al. The Lancet Neurology 2011;10(2):131-39
61. Hyperosmolar therapy
⢠Comparison of HTS and mannitol for severe TBI
⢠Alternating treatment strategy
⢠Randomization to decide initial agent
⢠Subsequently alternate with other agent
⢠Outcome: Decrease in ICP and duration of action
⢠Doses of similar osmotic burden used
⢠Mannitol 20% 2ml/kg versus HTS 15% 0.42ml/kg
⢠Mean âICP with mannitol 7.96mm versus HTS 8.43
⢠Duration: Mannitol 3hrs 33min versus HTS 4hrs 17mins
Sakellaridis et al. J Neurosurg 2011;114(2):545-8
62.
63. ⢠Objective: To assess the effect of mannitol given in different
does, in comparison with other agents, and to quantify effect
of mannitol when given at different stages of TBI
⢠RCTs of mannitol in TBI of any severity
⢠Mannitol better than pentobarbital
⢠Worse than HTS
⢠ICP directed use of mannitol-small beneficial effect on
neurological signs
⢠Insufficient data on usefulness in the pre-hospital setting
64. ⢠HTS versus Mannitol: A meta-analysis of RCTs
⢠Kamel and colleagues
⢠2011
⢠5 RCTs with 112 patients and 184 episodes of elevated ICP
⢠HTS better than mannitol for treating elevated ICP
⢠2mm mean difference between the two
⢠Limitations: small number and size of eligible trials
⢠Further studies needed
Kamel et al. Crit Care Med 2011;39(3):554-9
65. Prognostication
âIn TBI estimates of prognosis are unduly optimistic or
unnecessarily pessimistic or inappropriately ambiguousâ
Authors of CRASH trial
Early indicators of prognosis in severe TBI. Brain trauma foundation guidelines.
67. ⢠Issues with GCS
1. Optimal time after injury for determining GCS
2. When to assess if patient has received paralytics/sedatives
3. Reliability of pre-hospital GCS
⢠AGE
- Strong predictor of morbidity and mortality
- Children consistently do better
- Age above 60 poor prognosis
68.
69. ⢠Pupillary diameter
1. Diameter and light reflex studied extensively
2. In most studies accurate measurement not done
3. Duration of dilation and fixation must be documented
4. Hypotension and hypoxia must be corrected
5. Direct orbital trauma must be excluded
6. Pupils must be evaluated after surgical evacuation
70.
71. ⢠Hypotension
- Primary predictor of outcome
- One of the 5 most powerful predictors
- Single episode can double mortality
⢠CT Scan
- Status of basal cisterns
- SAH
- presence and degree of midline shift
- presence and type of intracranial lesions
72. Summary
⢠TBI is major problem with significant mortality and morbidity
⢠Affects the productive work force
⢠Pre-hospital management is crucial
⢠Guideline based management improves functional outcomes
and survival
⢠Neuromonitoring is important
⢠Maintaining cerebral oxygenation and hemodynamics is
critical
⢠Evidence on major aspects of TBI is consistently controversial
⢠Good clinical sense and common sense improves outcomes